Consequently, the bone marrow (BM) in tumour-bearing hosts is chronically exposed to mediators that can inhibit the expression and function of canonical transcription factors involved in the myeloid differentiation at steady state condition (i.e., CCAAT/enhancer binding protein α (c/EBPα)), thus skewing the activation of “emergency” haematopoiesis regulators such as c/EBPβ and IFN regulatory factor (IRF)8 and members of the signal transducer and activator of transcription (STAT) family such as STAT3, STAT1, and STAT6 [70,71,72,73]. This evidence concerns the gene STAT3 and neoplasm.